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L Cheng

Publications and source records attributed to L Cheng.

At least 163 records · Page 9Linked to original sources
PubMed1999

Hemangioma of the urinary bladder.

BACKGROUND: Hemangioma of the urinary bladder is rare and the long term outcome of patients is unknown. METHODS: The authors evaluated the clinical and pathologic findings in 19 patients with a vesical hemangioma. All patients were treated at the Mayo Clinic between 1932-1998 and had histologic confirmation of the diagnosis. Hemangioma was classified into cavernous, capillary, or arteriovenous types based on conventional criteria from other sites. Clinical information was obtained from chart review. The mean follow-up of the patients was 6.9 years (range, 0.3-25 years). RESULTS: The mean patient age at the time of diagnosis was 58 years (range, 19-76 years) and the male-to-female ratio was 3.7:1. Patients typically presented with macroscopic hematuria and endoscopic findings usually were nonspecific. The diagnosis of hemangioma was suspected in 3 patients (16%) prior to biopsy. There was a predilection for the posterior and lateral walls and the tumor usually was small (range, 0.2-3 cm; median, 0.7 cm) and solitary. The histologic types of hemangioma were cavernous (15 cases), capillary (2 cases), and arteriovenous (2 cases). All patients were treated with biopsy with or without fulguration, except for one patient who was treated with a partial cystectomy. No patients developed a recurrence during a mean follow-up of 6.9 years. CONCLUSIONS: Patients with hemangioma of the urinary bladder have a favorable outcome. Biopsy and fulguration are effective for hemangioma of the bladder when the lesion is small.

Adult↗
PubMed1999

Neurofibroma of the urinary bladder.

BACKGROUND: Neurofibroma of the urinary bladder is rare. Only isolated case reports have appeared. Information regarding the long term follow-up of patients with neurofibroma is limited. METHODS: The authors studied 4 cases of neurofibroma of the bladder diagnosed at Mayo Clinic from 1965 through 1990. Immunostains for S-100 protein, neurofilament protein, epithelial membrane antigen (EMA), cytokeratin (CAM 5.2; AE 1/3), Type IV collagen, MIB-1, and p53 protein were performed in all cases, as was Alcian blue at pH 2.5. The mean follow-up was 9.6 years (range, 2-18 years). RESULTS: The mean age at diagnosis was 17 years (range, 7-28 years); the male-to-female ratio was 1:1. All four patients exhibited physical stigmata of neurofibromatosis type 1. Clinical presentations included hematuria (one patient), irritative symptoms (two patients), and pelvic mass (one patient). Long term urinary complications included bladder atony (two patients), neurogenic bladder (one patient), and recurrent urinary tract infection with hematuria (one patient). Subsequently, two patients underwent partial cystectomy and one a complete cystectomy. Involvement of the bladder was generalized in all four cases. Three tumors were transmural, showing a diffuse and plexiform pattern of growth; in the fourth case, a superficial biopsy showed only diffuse submucosal growth with conspicuous pseudo-Meissnerian corpuscle formation. An Alcian blue positive, variably collagenized matrix was present in all cases. Tumor cells displayed immunoreactivity for S-100 protein and Type IV collagen in all cases. Neurofilament protein positive axons were evident in three cases; all other immunostains were negative. The mean MIB-1 labeling index was 3.2% (range, 0.9-7.3%). No malignant transformation was observed during a mean follow-up of 9.6 years. CONCLUSIONS: Neurofibroma of the bladder presents early in life, is of the plexiform type with a diffuse component, and usually occurs in the setting of generalized neurofibromatosis type 1 rather than as isolated visceral neurofibromatosis. Malignant transformation did not occur in any of these 4 patients during a mean follow-up time of 9.6 years.

Adolescent↗
PubMed1999

Glutathione-S-transferase polymorphisms and risk of squamous-cell carcinoma of the head and neck.

Differences in genetic susceptibility to tobacco-induced carcinogenesis appear to modulate an individual's risk of squamous-cell carcinoma of the head and neck (SCCHN). Risk for SCCHN may be associated with the null alleles of the carcinogen-metabolizing genes glutathione-S-transferase (GST) T1 and GSTM1. In this study, we evaluated the association between GSTM1 and GSTT1 null genotypes and risk of SCCHN in a matched case-control study of 162 patients with SCCHN and 315 healthy controls. Our results showed that 53.1% of cases and 42.9% of controls were null for GSTM1, whereas 32.7% of cases and 17.5% of controls were null for GSTT1 (p < 0.05 and p < 0.001, respectively). Furthermore, 19.8% of cases but only 7.9% of controls were null for both genes (p < 0.001). Multivariate analysis using logistic regression models, including age, sex, ethnicity, smoking status, alcohol status and GST genotypes, showed that both of these genotypes remained independent risk factors for disease [adjusted odds ratios (ORs) = 1.50 and 2.27, respectively; 95% confidence intervals (CIs) = 1.01-2.23 and 1.43-3.60, respectively). When the genotypes were divided into neither null, either null or both null, there was a dose-response relationship (adjusted OR = 1.50, 95% CI = 0.98-2.30) for the either-null group and (adjusted OR = 3.64, 95% CI = 1.94-6.84) for the both-null group (p < 0.001, trend test). Our findings suggest that the GSTM1 and GSTT1 null genotypes are independent risk factors for SCCHN and markers for genetic susceptibility to tobacco-induced carcinogenesis.

Adult↗
PubMed1999

Tumor size predicts the survival of patients with pathologic stage T2 bladder carcinoma: a critical evaluation of the depth of muscle invasion.

BACKGROUND: Accurate examination of radical cystectomy specimens is critical for stratifying patients into prognostically important groups and determining the need for adjuvant treatment. Evidence has accumulated that cancers invading the superficial muscle wall (T2a) behave similarly to those invading the deep muscle wall (T2b). Quantitative analysis of the depth of invasion in relation to patient outcome is needed. METHODS: The authors systematically evaluated the depth of invasion by micrometer measurement and its relation to the survival of 64 patients with bladder carcinoma pathologic classification as pT2 who had long term follow-up after radical cystectomy. Numerous clinical and pathologic variables were analyzed with univariate and multivariate Cox proportional hazards models. The mean age of patients was 64 years, and their mean follow-up was 8.3 years. RESULTS: There was no significant difference in clinical outcome between patients with T2a carcinoma and those with T2b. Lymph node metastasis and tumor size were each significantly associated with distant metastasis free and cancer specific survival. Ten-year distant metastasis free and cancer specific survival were 100% and 94%, respectively, for patients with tumors <3 cm (P = 0.006) and 68% and 73%, respectively, for patients with tumors > or = 3 cm (P = 0.005). After adjustment for lymph node status, tumor size maintained significance in predicting distant metastasis free survival (risk ratio, 1.5; 95% confidence interval, 1.1-2.0; P = 0.009) and cancer specific survival (risk ratio, 1.5; 95% confidence interval, 1.1-1.9; P = 0.01). Age was associated with recurrence free survival and all-cause survival. None of the other variables, including gender, vascular invasion, presence of carcinoma in situ, pathologic classification (T2a vs. T2b), depth of invasion, depth of muscle invasion, ratio of depth of invasion to bladder wall thickness, and percentage of muscle wall invasion, were significantly associated with patient outcome. CONCLUSIONS: The findings of this study indicate that the subclassification of T2 bladder carcinoma by depth of muscle invasion is of no prognostic value; conversely, tumor size, an easily measured factor, is predictive of distant metastasis free and cancer specific survival.

Adult↗
PubMed1999

p53 alteration in regional lymph node metastases from prostate carcinoma: a marker for progression?

BACKGROUND: Alterations of the p53 tumor suppressor gene are associated with advanced stage prostate carcinoma. The biologic significance of p53 nuclear accumulation in prostate cancer patients with regional lymph node metastases is uncertain. METHODS: The authors investigated p53 alterations by immunohistochemistry in 220 lymph node positive patients who were treated with radical prostatectomy, bilateral pelvic lymphadenectomy, and androgen deprivation therapy between 1987-1992 at the Mayo Clinic. The mean follow-up was 6.3 years. Tumor volume of lymph node metastases was measured using the grid method. RESULTS: p53 immunoreactivity was detected in 109 of 211 primary tumors (52%) and 83 of 144 matched regional lymph node metastases (58%); this expression was strongly concordant (correlation coefficient 0.53; P = 0.0001). Overexpression of p53 protein in lymph node metastases was associated with distant metastasis free survival by univariate analysis (P = 0.03), but did not reach statistical significance by multivariate analysis (P = 0.07). Regional lymph node cancer volume was the single most important predictor of distant metastases after adjusting for Gleason score, DNA ploidy, and p53 expression. CONCLUSIONS: The findings of the current study suggest that assessment of biologic changes (including p53 alterations in regional lymph node metastases) could be of value in the assessment of the biologic aggressiveness of prostate carcinoma, whereas p53 expression in the primary tumor does not appear to influence patient outcome.

Aged↗
PubMed1999

Survival of patients with carcinoma in situ of the urinary bladder.

BACKGROUND: To the authors' knowledge, the long term follow-up of patients with carcinoma in situ of the urinary bladder is limited. METHODS: The authors studied 138 patients diagnosed with urothelial carcinoma in situ of the bladder at the Mayo Clinic between 1972-1979. All the histologic slides were reviewed and fulfilled the diagnostic criteria for carcinoma in situ according to the newly proposed World Health Organization and International Society of Urologic Pathology classification system. None of these patients had previous or coexisting invasive urothelial carcinoma at the time of diagnosis. Cox proportional hazards models were used to determine the prognostic significance of numerous clinical and pathologic findings using progression free, cancer specific, and all-cause survival as the endpoints for analysis. Progression was defined as the development of invasive carcinoma, distant metastases, or death from bladder carcinoma. RESULTS: The patients ages at the time of diagnosis ranged from 32-90 years (mean, 65.6 years). The male to female ratio was 7:1. Carcinoma in situ usually was multifocal (50%) with a predilection for the trigone, lateral wall, and dome. The mean follow-up after surgery was 11.0 years (range, 0.7-25 years). Actuarial progression free, cancer specific, and all-cause survival rates were 63%, 79%, and 55%, respectively, at 10 years, and 59%, 74%, and 40%, respectively, at 15 years. The mean interval from the time of diagnosis to cancer progression was 5 years. Patient age at diagnosis was significant in predicting progression free (P = 0.01) and all-cause survival (P = 0.002). Cystectomy performed within 3 months after the initial diagnosis was associated with improved all-cause survival (P = 0.03). After controlling for age, there was no difference in survival between patients who received immediate cystectomy and those did not (P = 0.16). CONCLUSIONS: Patients with carcinoma in situ of the bladder are at significant risk of cancer progression and death from bladder carcinoma. Cystectomy does not appear to offer a significant survival advantage in patients with carcinoma in situ of the bladder after adjusting for age.

Adult↗
PubMed1999

Allelic imbalance in the clonal evolution of prostate carcinoma.

BACKGROUND: To understand better the genetic basis of the clonal evolution of prostate carcinoma, the authors analyzed the pattern of allelic loss in 25 matched primary and metastatic prostate tumors. METHODS: Twenty-five cases were selected from the surgical pathology files of the Mayo Clinic from patients who had undergone radical retropubic prostatectomy and bilateral lymphadenectomy between 1987-1991. All patients had regional lymph node metastases at the time of surgery. DNA samples for the analysis of allelic loss pattern were prepared from primary tumors and matched synchronous lymph node metastases by tissue microdissection. The oligonucleotide primer pairs for the microsatellite DNA markers were D8S133, D8S136, D8S137, ANK1 on chromosome 8p12-21, LPLTET on chromosome 8p22, and D17S855 (intragenic to the BRCA1 gene) on chromosome 17q21. One case was not informative at any of the loci tested and was excluded from further analysis. RESULTS: The overall frequency of allelic imbalance was 79% in primary tumors and 88% in paired metastases. Of 24 informative cases, 14 patients (58%) showed the same pattern of allelic loss or retention in matched primary and metastatic tumors at all marker locus; discordant allelic loss was observed in the remaining 10 patients (42%). Four patients showed loss of the same allele at one or more marker loci in both primary and metastatic tumors, but discordant allelic loss was observed at other marker loci. Five patients showed allelic loss in at least one genetic marker in the metastatic tumor but not in its matched primary tumor. Five patients displayed loss of one allele at one or more marker loci in a primary tumor but not in the matched metastases. There was no significant difference in the frequency of allelic imbalance between primary and metastatic tumors at any marker analyzed (P>0.05). CONCLUSIONS: These data suggest that different patterns of allelic deletion may be acquired during cancer progression to metastases. The differences in genetic composition between primary prostate carcinoma and its metastases may be related to intrinsic cancer heterogeneity, overall genetic instability, and clonal divergence.

Aged↗
PubMed1999

Predictors of cancer progression in T1a prostate adenocarcinoma.

BACKGROUND: The biologic behavior of T1a prostate adenocarcinoma is variable. A critical issue in the management of patients with T1a prostate adenocarcinoma is to distinguish those who will develop cancer progression from those who will not. Predictive factors that identify those at high risk of cancer progression are needed to stratify patients for treatment. In the current study the authors attempted to identify such predictors of cancer progression in a large series of untreated patients with lengthy follow-up. METHODS: The authors studied 102 patients who were diagnosed with T1a prostate adenocarcinoma (incidental tumor involving < or = 5% of the resected prostatic tissue) at the time they underwent transurethral resection of the prostate (TURP) at the Mayo Clinic between 1960-1970. None of these patients were treated. Patient ages ranged from 48-91 years (mean +/- standard deviation, 69 +/- 7 years). The average weight of the resected prostate tissue was 24 +/- 18 g (range, 3-115 g; median, 18 g). Tumor volume was measured by the grid method. Cox proportional hazards models were used to identify factors associated with cancer progression. Survival curves were estimated using the Kaplan-Meier method. RESULTS: Five-year and 10-year progression free survival rates were 93% and 87%, respectively. During the mean follow-up of 9.5 +/- 6.8 years (range, 0.3-31 years; median, 9.0 years), 14 patients developed clinical cancer progression, including 5 patients with systemic progression (1 with distant metastases and 4 who died of prostate adenocarcinoma). The interval from diagnosis to clinical cancer progression ranged from 1-23 years (mean, 7.3 years). The amount of resected prostate tissue (TURP weight) was associated with progression (P = 0.04). Patients with a TURP weight > or = 30 g had 100% progression free survival at 10 years compared with a progression free survival rate of 73% in patients with a TURP weight < 12 g. Gleason score, tumor volume, number of chips involved by tumor, number of tumor foci, and the presence of high grade prostatic intraepithelial neoplasia were not significant in predicting cancer progression. There was a trend toward a worse prognosis with the increasing number of chips involved by cancer (P = 0.16). Patients with < 3 chips involved by cancer had a 88% 10-year progression free survival rate compared with 73% in patients with > or = 3 chips involved by cancer. CONCLUSIONS: The clinical course of T1a prostate adenocarcinoma is variable. If left untreated, a small but significant proportion of patients are at risk for disease progression and death. However, the current study found that patients with a TURP weight > or = 30 g have an excellent prognosis and can be managed conservatively.

Adenocarcinoma↗
PubMed1999

p53 protein overexpression is associated with increased cell proliferation in patients with locally recurrent prostate carcinoma after radiation therapy.

BACKGROUND: The biologic changes in recurrent prostate carcinoma following radiation therapy are not fully understood. The authors sought to determine the level of p53 protein overexpression and its association with cellular proliferation (Ki-67 labeling index), glutathione S-transferase-pi (GST-pi) expression, and other clinical pathologic findings in patients with locally persistent prostate carcinoma after radiation therapy. METHODS: The authors investigated p53 nuclear accumulation, cellular proliferation activity (Ki-67 labeling index by digital image analysis), and GST-pi expression in 55 patients with persistent or recurrent prostate carcinoma after radiation therapy. All patients underwent salvage radical prostatectomy and bilateral pelvic lymphadenectomy following irradiation failure. The interval from radiation therapy to cancer recurrence ranged from 6 months to 17 years (mean, 3.8 years). Age at surgery ranged from 51 to 78 years (mean, 65 years). Mean follow-up after surgery was 5.7 years (range, 1-13 years). RESULTS: p53 protein overexpression was associated with increased cell proliferation (Spearman rank correlation coefficient = 0.29, P = 0.03). A substantial proportion (62%) of recurrent cancer also showed GST-pi immunoreactivity. No apparent correlation was observed between p53 protein overexpression, cellular proliferation (Ki-67 labeling index), or GST-pi expression and Gleason score, pathologic stage, DNA ploidy, or patient outcome. There was an inverse correlation between GST-pi expression and Gleason score (P = 0.06). The majority of prostate carcinomas (95%) were proliferative (mean Ki-67 labeling index, 7.0; range, 0-20), whereas concurrent prostatic intraepithelial neoplasia (PIN) had a lower Ki-67 labeling index (mean, 3.1; range, 0-11.5). Nineteen of 28 (68%) concurrent PIN demonstrated p53 immunoreactivity. A trend toward adverse clinical outcome was observed in patients with a higher Ki-67 labeling index in recurrent cancer. CONCLUSIONS: In this study cohort selected for salvage prostatectomy, recurrent cancers were biologically aggressive following radiation therapy. Whether this represents selective persistence and regrowth of prognostically unfavorable tumor clonogens or stepwise clonogenic progression is uncertain. Further investigation is needed to elucidate the correlation between p53 overexpression and the presence of other biologic changes after radiation therapy.

Aged↗
PubMed1999

Overexpression of the wild type p73 gene in human bladder cancer.

p73, a first p53 relative, was recently identified and shown to be monoallelically expressed in a number of different human tissues. To determine the potential role of this gene in human bladder cancer, we investigated p73 expression levels, allelic expression patterns, and analysed p73 mutations in 23 unselected primary invasive bladder cancers with matched normal tissues and in seven bladder cancer cell lines. In a comparison between normal and tumor tissues using quantitative RT-PCR analysis, we found that p73 was overexpressed in 22/23 bladder cancers, sometimes as great as 20-fold. Allelic expression analysis using a C/T polymorphism in exon 2 and a newly identified T/C polymorphism in exon 5 revealed that p73 was biallelically expressed in both normal bladder and cancer tissues, suggesting that p73 is not imprinted in bladder tissue. Mutation screening of the p73 gene in bladder cancer DNAs using denaturing high-performance liquid chromatography analysis and DNA sequencing revealed no tumor-specific mutations in any coding exons of the p73 gene. These data suggest that the p73 is unlikely to be a tumor suppressor gene, but that overexpression of p73 may contribute to tumorigenesis in bladder cancer.

Alleles↗
PubMed1999

Weak organic acid treatment causes a trehalose accumulation in low-pH cultures of Saccharomyces cerevisiae, not displayed by the more preservative-resistant Zygosaccharomyces bailii.

Weak organic acid food preservatives exert pronounced culture pH-dependent effects on both the heat-shock response and the thermotolerance of Saccharomyces cerevisiae. In low-pH cultures, they inhibit this stress response and cause strong induction of respiratory-deficient petites amongst the survivors of lethal heat treatment. In higher pH cultures, 25 degrees C sorbic acid treatment causes a strong induction of thermotolerance without inducing the heat-shock response. In this study we show that trehalose, a major stress protectant, accumulates rapidly in S. cerevisiae exposed to sorbate at low pH. In pH 3.5 cultures, a 25 degrees C sorbate treatment is as effective as a 39 degrees C heat shock in inducing trehalose. This weak-acid-induced trehalose accumulation is enhanced in the pfk1 S. cerevisiae mutant, indicating that it arises through inhibition of glycolysis at the phosphofructokinase step. The more preservative-resistant food spoilage yeast Zygosaccharomyces bailii differs from S. cerevisiae in that: (1) its basal thermotolerance is not strongly affected by culture pH; (2) it does not display trehalose accumulation in response to 25 degrees C sorbate treatment at low pH; and (3) there is no induction of respiratory-deficient petites during lethal heating with sorbate. This probably reflects Z. bailii being both petite-negative and better equipped for maintenance of homeostasis during weak-acid, pH or high-temperature stress.

Food Preservatives↗
PubMed1999

Mutation and expression analysis of the p73 gene in prostate cancer.

BACKGROUND: p53 is the most highly mutated tumor suppressor gene in human cancers. Recently, p73, a first homologue of p53, was identified and considered to be an imprinted tumor suppressor gene. Thus, we analyzed the possible role of p73 in human prostate cancers. METHODS: We investigated the expression levels and expressed allelotypes and searched for mutations in the p73 gene in 27 primary prostate cancers with matched normal tissues as well as in four prostate cell lines. RESULTS: Allelic expression analysis using polymorphisms in exons 2 and 5 revealed that p73 is biallelically expressed in both normal and tumor tissues, suggesting that p73 is not imprinted in prostate tissues. Quantitative PCR demonstrated that p73 expression is the same in both normal and tumor prostate tissues. Denaturing high-performance liquid chromatography and DNA sequencing revealed that there were no tumor-specific mutations in the p73 gene at the genomic level. CONCLUSIONS: These data indicate that alterations of p73, including mutations, changes in message abundance, and changes in allelic expression, are likely to be rare in early-stage prostate cancer, and that p73 could be a tissue-specific imprinting gene.

DNA Mutational Analysis↗
PubMed1999

Cloning and analysis of small cytoplasmic leucine-rich repeat protein (SCLP), a novel, phylogenetically-conserved protein that is dramatically up-regulated during the programmed death of moth skeletal muscle.

We used the abdominal intersegmental muscles (ISMs) of the moth Manduca sexta as a source of transcripts that are dramatically up-regulated during programmed cell death. One of these transcripts, Small Cytoplasmic Leucine-Rich Repeat Protein (SCLP), encodes a protein of approximately 24 kD that contains four perfect and two imperfect leucine-rich repeat (LRR) motifs. DNA sequence database analysis suggests that SCLP is a phylogenetically-conserved gene of unknown function. Both Northern and Western blots demonstrated that SCLP is expressed in the ISMs at all stages examined, but increases greater than 10-fold when the cells become committed to die. This increase in expression is regulated by the same change in the circulating ecdysteroid titer that controls death. Low levels of SCLP expression are also seen in flight muscle and fat body, but not in ovary, male sexual accessory gland, or Malpighian tubules. Immunohistochemical analysis demonstrates that SCLP is a cytoplasmic protein. Western blot analysis of proteins from the fly Drosophila suggests that an SCLP-related protein is expressed at the larval and pupal stages, but not in embryos or adults. Targeted expression of moth SCLP to a variety of different tissues in Drosophila using the Gal4/UAS P element system failed to generate an overt phenotype. These data are interpreted as suggesting that whereas SCLP presumably plays an important role in programmed cell death of muscle, perhaps by acting as an adaptor protein, its expression is insufficient to initiate death by itself.

Amino Acid Sequence↗
PubMed1999

Evaluation of the human choroidal melanoma rabbit model for studying microcirculation patterns with confocal ICG and histology.

The aim of this study was to develop consistently focal elevated choroidal masses of human choroidal melanoma in immunosuppressed rabbits and to correlate the visualization of prognostically significant microcirculation patterns from confocal indocyanine green angiography with histologic microcirculation patterns. A human choroidal melanoma cell line (OCM1) was implanted in the choroid of 40 rabbit eyes using three different techniques: transscleral choroidal injection of a cell suspension, injection of a cell suspension in a surgically induced cyclodialysis cleft, and implantation of solid tumor fragments in a surgically induced cyclodialysis cleft. The rabbits were immunosuppressed with daily injections of Cyclosporin A to prevent host versus graft reaction. The eyes were studied weekly with indirect ophthalmoscopy and fundus photography to monitor tumor growth and indocyanine green angiography using a confocal scanning laser ophthalmoscope to identify microcirculation patterns in vivo and correlate these findings with the histologic demonstration of tumor microcirculation patterns. A tumor mass was identified by indirect ophthalmoscopy in 16 of the 40 implanted rabbit eyes (40%). Each of these tumors was confirmed histologically to represent a focal elevated choroidal mass. All 16 elevated choroidal masses grow in eyes in which solid tumor fragments were implanted. In total, a melanoma was identified histologically in 28 of the implanted 40 eyes (70%). In addition to the 16 eyes where the melanoma appeared as a focal elevated choroidal mass, 4 eyes contained a focal elevated mass in the sclera and 8 eyes contained a flat choroidal tumor. Histologically, microcirculation patterns were identified only in the 16 eyes with focal elevated choroidal masses. Confocal indocyanine green angiography imaged microcirculation patterns in 13 of these 16 eyes (81%). The surgical implantation of small solid fragments of human choroidal melanoma in immunosuppressed rabbit eyes provides the best method to consistently obtain focal elevated choroidal masses. These focal elevated choroidal masses resemble booth the localization and the growth pattern of choroidal melanomas in humans. In addition, they also contain microcirculation patterns similar to those seen in humans that are detectable with confocal indocyanine green angiography. The use of indocyanine green angiography with this animal model may be especially useful in designing and evaluating anti-microcirculation treatments directed at uveal melanoma.

Angiography↗
PubMed1999

Acute exercise enhances receptor-mediated endothelium-dependent vasodilation by receptor upregulation.

The effects of acute exercise on receptor-mediated endothelium-dependent vasodilation and its possible mechanisms were investigated in the presence of indomethacin. Male Wistar rats (16-20 weeks old) were divided into control and exercise groups. The exercise group ran on a drum exerciser until exhaustion, followed by immediate decapitation. Acetylcholine (ACh)- or clonidine (CLO)-induced vasodilating responses in thoracic aortae of the control and exercise groups were compared. Receptor-binding assays were performed to determine whether there were any upregulations of endothelial receptors after acute exercise. Our results indicated that acute exercise induced the following effects: (1) the dose-response curves of ACh and CLO shifted to the left; (2) the high-affinity M3 binding sites increased in number but not in affinity; (3) the alpha2 binding sites decreased in number but increased in affinity. We conclude that acute exercise enhances receptor-mediated vasodilation responses, at least in part, by regulating either endothelial receptor number or receptor affinity.

Acetylcholine↗
PubMed1999

Effect of terazosin on blood pressure and serum lipids.

In an open multicenter prospective study, the effects of short-term (4 weeks, n = 101) and long-term (6 months, n = 38) terazosin treatment on blood pressure, serum lipids and safety in the patients with mild to moderate essential hypertension were observed. Mean systolic and diastolic blood pressure in sitting position were significantly reduced by 16.4% and 14.0% respectively (P < 0.01) after 4 weeks of terazosin therapy, with the total efficacy rate being 87.1%. During a 6 month therapy, antihypertensive effect of terazosin could be maintained. Total cholesterol (TC) and low density lipoprotein (LDL) cholesterol in serum were significantly decreased P < 0.05-0.01) in patients with hypercholesterolemia (TC > or = 6 mmol/ml) after 4 week terazosin treatment; the levels of TC, LDL and triglyceride were significantly improved in hypertensive patients after 3-6 month terazosin treatment. The improvement of lipid metabolism was related to the dosage of terazosin but not to antihypertensive effects of terazosin. The results suggested that terazosin is effective in decreasing blood pressure and improving lipid metabolism. It may serve as a good antihypertensive agent for hypertensive patients with hypercholesterolemia.

Antihypertensive Agents↗
PubMed1999

Cystic renal cell carcinoma is cured by resection: a study of 24 cases with long-term followup.

PURPOSE: The true incidence and biological behavior of cystic renal cell carcinoma are not known. To our knowledge we present the largest series of patients with cystic renal cell carcinoma with long-term followup. MATERIALS AND METHODS: We reviewed the Mayo Clinic surgical pathology files of renal cell cancer cases with a cystic component resected from 1969 to 1997, and arbitrarily chose 75% tumor involvement by cysts as a cutoff for inclusion in the study. RESULTS: We identified 24 cases of clear cell renal cell carcinoma with 75% or greater involvement by cysts comprising 0.79% of 3,047 renal cell cancer cases resected at our institution between 1969 and 1997. Mean patient age was 62.7 years (range 40 to 83). A total of 11 patients (46%) underwent radical nephrectomy, 4 (17%) simple nephrectomy, 3 (12%) partial nephrectomy and 6 (25%) tumor enucleation. Mean tumor involvement by cysts was 84% (range 75 to 95) and in 11 cases (46%) involvement was 90% or greater. Cancer stage was T1 in 20 patients (83%), T2 in 1 (4.4%) and T3a in 4 (12.5%). Cancers were diploid in all but 1 case. Mean followup was 77.6 months (range 8 to 428, median 51). A total of 22 patients (92%) had no evidence of cancer and 2 died of intercurrent disease. CONCLUSIONS: Our results indicate that cystic renal cell carcinoma is uncommon and usually cured by resection, regardless of size, stage or number of cysts. These patients may benefit from nephron sparing surgery, such as partial nephrectomy.

Adult↗